Evidence map›Paper›PMID 32021297›Full record

ArticleOncoTargets and therapy2020

circGFRA1 Enhances NSCLC Progression by Sponging miR-188-3p.

Jie Yao, Guanxin Xu, Ling Zhu, Heqing Zheng

Abstract read
In one paragraph

Article in OncoTargets and therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

29 citing papers in PubMed.

  1. Review
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  8. Circular RNAs as biomarkers for lung cancer.Non-coding RNA research · 2023
    Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors.

Jie YaoDepartment of Thoracic Surgery, Second Affiliated Hospital of Zhejiang University, School of Medicine, Hangzhou 310009, People's Republic of China.ORCID 0000-0003-0818-3721
Guanxin XuDepartment of Thoracic Surgery, Second Affiliated Hospital of Zhejiang University, School of Medicine, Hangzhou 310009, People's Republic of China.
Ling ZhuDepartment of Thoracic Surgery, Second Affiliated Hospital of Zhejiang University, School of Medicine, Hangzhou 310009, People's Republic of China.
Heqing ZhengDepartment of Thoracic Surgery, Yueqing People's Hospital, Wenzhou, People's Republic of China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundLung cancer continues to be one of the most dangerous tumors around the world. It is an urgency to explore the molecular mechanism of non-small cell lung cancer (NSCLC) progression for developing novel therapeutic approaches. Circular RNA (circRNA) is a novel type of non-coding RNA with a stable closed loop structure. Abnormally expressed circRNAs have been found in many kinds of cancer including NSCLC. METHODS AND

resultsThe expression of circGFRA1 and miR-188-3p was detected in NSCLC tissues by RT-qPCR and it was found that circGFRA1 was highly expressed and miR-183-3p was lowly expressed in NSCLC tissues. In NSCLC cell lines, we confirmed that circGFRA1 acted as an miR-188-3p sponge using dual-luciferase reporter assay and RNA immunoprecipitation (RIP) analysis. Overexpression of cirGFRA1 enhanced NSCLC progression while miR-188-3p overexpression inhibited it by CCK8 and colony formation analysis. In vivo tumor xenograft model, circGFRA1 and miR-188-3p synergistically regulated the proliferation of NSCLC tumors. Mechanistic study indicated that circGFRA1 and miR-188-3p regulated the proliferation of NSCLC cells at least through PI3K/AKT signaling pathway.

conclusionOur study elaborated a novel circGFRA-miR-188-3p-PI3K/AKT regulatory pathway, providing a potential diagnostic biomarker and therapeutic target for NSCLC.

Indexed as

circGFRA1miR-188-3pNSCLCPI3K/AKT

Identifiers

PMID32021297
PMCPMC6980840

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.